The goals of scale-up of antiretroviral therapy (ART) have expanded from prevention of morbidity and death to include prevention of transmission. Morbidity and mortality risk are associated with CD4 count; transmission risk depends on plasma viral load (VL). This study aimed to describe CD4 count and VL distributions among HIV-infected individuals in a South African township to gain insights into the potential impact of ART scale-up on community HIV transmission risk.
A random sample of 10% of the adult population was invited to attend an HIV testing service. Study procedures included a questionnaire, HIV testing, CD4 count, and VL testing.
One thousand one hundred forty-four (88.0%) of 1300 randomly selected individuals participated in the study. Two hundred sixty tested positive, giving an HIV prevalence of 22.7% [95% confidence interval (CI): 20.3 to 25.3]. A third of all HIV-infected individuals (33.5%, 95% CI: 27.8 to 39.6) reported taking ART. The median CD4 count was 417 cells per microliter (interquartile range, 285–627); 33 (12.7%, 95% CI: 8.9 to 17.4) had a CD4 count of ≤200 cells per microliter. VL measurements were available for 219 individuals (84.2%) and were undetectable in 72 (33.9%), >1500 copies per milliliter in 127 (58.0%) and >10,000 copies per milliliter in 96 (43.8%). Of those reporting they were receiving ART, 30.4% had a VL >1500 copies per milliliter compared with 58.0% of those reporting they were not receiving ART.
A small proportion of those living with HIV in this community had a CD4 count of <200 cells per microliter; more than half had a VL high enough to be associated with considerable transmission risk. A substantial proportion of HIV-infected individuals remained at risk of transmitting HIV even after starting ART.
Supplemental Digital Content is Available in the Text.
*Department of Clinical Research, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, London, United Kingdom;
†The Desmond Tutu HIV Centre, Institute for Infectious Disease and Molecular Medicine, Faculty of Health Science, University of Cape Town, Cape Town, South Africa;
‡Centre for Infectious Disease Epidemiology and Research, University of Cape Town, Cape Town, South Africa; and
§Department of Medicine, Faculty of Health Science, University of Cape Town, Cape Town, South Africa.
Correspondence to: Katharina Kranzer, Department of Clinical Research, Faculty of Infectious and Tropical Diseases, London School of Hygiene and Tropical Medicine, Keppel Street, WC1E 7HT London, United Kingdom (e-mai: firstname.lastname@example.org).
K. K. (087262/Z/08/Z) and S. D. L. (088590/Z/09/Z) are funded by the Wellcome Trust, London, United Kingdom. R. W. is funded by IeDEA (International epidemiologic databases to evaluate AIDS) and CEPAC (Cost-effectiveness of Preventing AIDS Complications). L.-G. B. is funded by the National Institutes of Health CIPRA (Comprehensive International Program for Research on AIDS).
The authors have no conflicts of interest to disclose.
Supplemental digital content is available for this article. Direct URL citations appear in the printed text and are provided in the HTML and PDF versions of this article on the journal's Web site (www.jaids.com).
Received November 26, 2012
Accepted February 21, 2013